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Published on: October 17, 2017
Intermediate monocytes are associated with the first major adverse cardiovascular event in patients with stable
Mihaela I Dregoesc1, Adrian B Țigu2, Siroon Bekkering3
1"Iuliu Hatieganu" University of Medicine and Pharmacy, Department of Cardiology - "Niculae Stancioiu" Heart Institute, Cluj-Napoca, Romania.
Insights
Intermediate monocytes predict major adverse cardiovascular events in patients with coronary artery disease (CAD). Classical monocytes showed a protective effect, independent of cytokine production, suggesting new biomarker potential for atherosclerosis risk stratification.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Biomarker Discovery
Background:
- Traditional risk stratification for cardiovascular events in coronary artery disease (CAD) has limitations.
- Investigating novel biomarkers like monocyte subsets may improve risk prediction.
Purpose of the Study:
- To examine the association between monocyte subsets (classical, intermediate, non-classical) and their function with major adverse cardiovascular events (MACE) in stable CAD patients.
- To determine if monocyte subset numbers or cytokine production capacity predict cardiovascular outcomes.
Main Methods:
- Flow cytometry was used to quantify monocyte subsets in 229 stable CAD patients.
- Ex-vivo stimulation assessed cytokine production capacity of peripheral blood mononuclear cells.
- Patients were followed for four years for MACE (cardiovascular death, myocardial infarction, ischemic stroke).
Main Results:
- A higher percentage of intermediate monocytes was significantly associated with increased MACE (HR 1.09; p=0.006).
- A higher percentage of classical monocytes was associated with a protective effect against adverse outcomes (HR 0.96; p=0.02).
- Intermediate monocyte association with MACE remained significant after adjusting for clinical factors (HR 1.07; p=0.04); cytokine production was not linked to outcomes.
Conclusions:
- Intermediate monocyte percentage is an independent predictor of MACE in stable CAD patients.
- This association is not explained by altered cytokine production capacity.
- Monocyte subsets represent potential novel biomarkers for improving risk stratification and therapeutic targets in atherosclerosis.
Background:
Traditional risk stratification modestly predicts adverse cardiovascular events in patients with coronary artery disease (CAD). Our aim was to investigate the association between monocyte subsets numbers and function, and the first major adverse cardiovascular event (MACE) in patients with symptomatic stable CAD and angiographically documented coronary atherosclerosis.
Methods:
Patients with stable CAD were screened for inclusion. Using flow cytometry, we identified classical, intermediate, and non-classical monocyte subsets and we assessed cytokine production capacity after ex-vivo stimulation of peripheral blood mononuclear cells. Clinical follow-up was performed after four years. The endpoint was the composite of cardiovascular death, acute myocardial infarction, and ischemic stroke.
Results:
A cohort of 229 patients was recruited. The percentage of intermediate monocytes was positively associated with adverse cardiovascular events at follow-up (HR 1.09; 95%CI 1.02-1.16; p = 0.006), while the percentage of classical monocytes was identified as a protective factor for adverse outcomes (HR 0.96; 95%CI 0.94-0.99; p = 0.02). The percentage of intermediate monocytes remained independently associated with outcomes after adjusting for age, systolic blood pressure, and left ventricular ejection fraction (HR 1.07; 95% CI 1.01-1.14; p = 0.04). Several correlations were identified between monocyte subsets and stimulated cytokine production, but cytokine production capacity was not associated with adverse outcomes.
Conclusions:
In patients with stable CAD, intermediate monocytes were associated with MACE at follow-up. The association was not due to an increased cytokine production capacity. Novel biomarkers could improve risk stratification in patients with stable CAD and could represent new pharmacological targets against atherosclerosis progression.
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